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Myeloperoxidase serves as a redox switch that regulates apoptosis in epithelial ovarian cancer

Ghassan M Saed1, Rouba Ali-Fehmi, Zhong L Jiang

  • 1Department of Obstetrics and Gynecology, The C.S. Mott Center for Human Growth and Development, Wayne State University School of Medicine, Detroit, MI 48201, USA. gsaed@med.wayne.edu

Gynecologic Oncology
|December 8, 2009
PubMed
Abstract

Insights

Myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) drive cancer cell survival in epithelial ovarian cancer (EOC) by inhibiting apoptosis. Silencing MPO or iNOS boosts apoptosis, suggesting their potential as therapeutic targets.

Area of Science:

  • Oncology
  • Biochemistry
  • Molecular Biology

Background:

  • Resistance to apoptosis is a hallmark of cancer, often regulated by S-nitrosylation.
  • Myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) produce nitrosonium ions (NO(+)) that mediate S-nitrosylation.
  • Investigating MPO and iNOS in epithelial ovarian cancer (EOC) is crucial for understanding apoptosis regulation.

Purpose of the Study:

  • To investigate MPO and iNOS expression in EOC.
  • To determine the role of MPO and iNOS in regulating S-nitrosylation of caspase-3, its activity, and apoptosis in EOC.
  • To explore MPO and iNOS as potential therapeutic targets in EOC.

Main Methods:

  • Immunofluorescence was used to assess MPO and iNOS expression in EOC cell lines and tissues.
  • Gene silencing of MPO and iNOS was performed using siRNA.
  • Real-time RT-PCR, ELISA, and TUNEL assays were employed to evaluate S-nitrosylation, caspase-3 activity, and apoptosis.

Main Results:

  • MPO and iNOS were expressed in EOC cell lines and invasive EOC tissues, but not in normal ovarian epithelium.
  • Silencing MPO or iNOS decreased caspase-3 S-nitrosylation and increased caspase-3 activity and apoptosis.
  • Silencing MPO demonstrated a more significant effect on inducing apoptosis compared to silencing iNOS.

Conclusions:

  • MPO and iNOS are co-expressed in EOC cells and play a critical role in regulating apoptosis.
  • MPO and iNOS act as redox switches controlling apoptosis in EOC.
  • Targeting MPO and iNOS may offer novel diagnostic and therapeutic strategies for EOC.

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